ArticleJournal of bacteriology2010
FliZ regulates expression of the Salmonella pathogenicity island 1 invasion locus by controlling HilD protein activity in Salmonella enterica serovar typhimurium.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 108 citations in OpenAlex.
- Bacterial chromatin remodeling associated with transcription-induced domains at pathogenicity Islands.Nature communications · 2026Article
- A Small RNA Derived From the 5' End of the IS200 tnpA Transcript Regulates Multiple Virulence Regulons in Salmonella typhimurium.Molecular microbiology · 2025Article
- HilE mediates motility thermoregulation in typhoidal Salmonella serovars at elevated physiological temperatures.PLoS pathogens · 2025Article
- TheJournal of bacteriology · 2025Article
- Controlling intracellular protein delivery, tumor colonization and tissue distribution using flhDC in clinically relevant ΔsseJ Salmonella.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Suppression of amber stop codons impairs pathogenicity in Salmonella.FEBS letters · 2025Article
- ThebioRxiv : the preprint server for biology · 2024Article
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- Epigallocatechin gallate protects mice fromFrontiers in cellular and infection microbiology · 2024Article
- Small RNAs Activate Salmonella Pathogenicity Island 1 by Modulating mRNA Stability through theJournal of bacteriology · 2023Article
- Measurement of Salmonella enterica Internalization and Vacuole Lysis in Epithelial Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Two Additional Connections between the Transcriptional Programs Controlling Invasion and Intracellular Replication of Salmonella: HilD-SprB Positively RegulatesJournal of bacteriology · 2022Article
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- The Small RNA MicC DownregulatesJournal of bacteriology · 2022Article
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- Intracellular delivery of protein drugs with an autonomously lysing bacterial system reduces tumor growth and metastases.Nature communications · 2021Article
- YeiE Regulates Motility and Gut Colonization in Salmonella enterica Serotype Typhimurium.mBio · 2021Article
- An incoherent feedforward loop formed by SirA/BarA, HilE and HilD is involved in controlling the growth cost of virulence factor expression by Salmonella Typhimurium.PLoS pathogens · 2021Article
- HilE is required for synergistic activation of SPI-1 gene expression in Salmonella enterica serovar Typhimurium.BMC microbiology · 2021Article
- Single Cell Analysis of Bistable Expression of Pathogenicity Island 1 and the Flagellar Regulon inMicroorganisms · 2021Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A prerequisite for Salmonella enterica to cause both intestinal and systemic disease is the direct injection of effector proteins into host intestinal epithelial cells via a type three secretion system (T3SS); the T3SS genes are carried on Salmonella pathogenicity island 1 (SPI1). These effector proteins induce inflammatory diarrhea and bacterial invasion. Expression of the SPI1 T3SS is tightly regulated in response to environmental signals through a variety of global regulatory systems. We have previously shown that three AraC-like regulators, HilD, HilC, and RtsA, act in a complex feed-forward regulatory loop to control the expression of the hilA gene, which encodes the direct regulator of the SPI1 structural genes. In this work, we characterize a major positive regulator of this system, the flagellar protein FliZ. Through genetic and biochemical analyses, we show that FliZ posttranslationally controls HilD to positively regulate hilA expression. This mechanism is independent of other flagellar components and is not mediated through the negative regulator HilE or through FliZ-mediated RpoS regulation. We demonstrate that FliZ controls HilD protein activity and not stability. FliZ regulates HilD in the absence of Lon protease, previously shown to degrade HilD. Indeed, it appears that FliZ, rather than HilD, is the most relevant target of Lon as it relates to SPI1 expression. Mutants lacking FliZ are significantly attenuated in their ability to colonize the intestine but are unaffected during systemic infection. The intestinal attenuation is partially dependent on SPI1, but FliZ has additional pleiotropic effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.